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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article is devoted to hormonal pathogenesis of chosen autoimmune diseases--systemic lupus erythematosus and systemic sclerosis--basis of the latest literature. Authors take note of possible role of many different hormonal factors, especially estrogens, androgens and prolactin, in etiology of these diseases. The further study of mentioned problems can lead to new clinical and therapeutic implications in dermatology and rheumatology.
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PMID:[Hormones--underestimated problem in dermatology. Part 2. Autoimmune disease]. 1236 80

Prolactin is a peptide hormone produced by the anterior pituitary gland that is critical in lactation. Prolactin can also be produced by lymphocytes, and both B and T cells express prolactin receptors. These findings have suggested that prolactin has immunomodulatory functions. Studies in spontaneously autoimmune hosts have demonstrated a role for prolactin in augmenting autoreactivity. We chose to analyze prolactin effects on anti-DNA B cells in nonspontaneously autoimmune female BALB/c mice transgenic for the heavy chain of an anti-DNA antibody. Treatment with prolactin for 4 weeks induced a lupus-like phenotype with an increased number of transgene-expressing B cells, elevated serum anti-DNA antibody titers, and glomerular immunoglobulin deposits. Prolactin caused a decrease in the population of transitional B cells and an increase in mature follicular and marginal zone B cells. The DNA-reactive B cells had a follicular cell phenotype. Anti-DNA hybridomas demonstrated that prolactin alters selection of the naive B cell repertoire. The expansion and activation of anti-DNA B cells in prolactin-treated R4A-gamma2b BALB/c mice was dependent on the presence of CD4(+) T cells. Finally, treatment with prolactin was unable to break tolerance in R4A-gamma2b transgenic C57Bl/6 mice, suggesting that responsiveness of the immune system to prolactin is genetically determined.
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PMID:Prolactin modulates the naive B cell repertoire. 1253 84

Genes encoding for prolactin (PRL) and its receptor (PRLR) are possible candidates for multiple sclerosis (MS) and systemic lupus erythematosus (SLE) susceptibility. In fact: (1) a prolactin secretion dysfunction has been described in several autoimmune diseases including SLE and MS and their animal models; (2) both PRL and PRLR are structurally related to members of the cytokine/hematopoietin family and have a role in the regulation of the immune response; and (3) both PRL and PRLR genes map in genomic regions that showed linkage with autoimmunity. Prolactin maps on chromosome 6p, about 11-kb telomeric to HLA-DRB1 and PRLR in 5p12-13, which revealed evidence of linkage with MS in different populations. To evaluate a possible role of these two genes in SLE and MS we performed an association study of 19 PRL and PRLR single nucleotide polymorphisms (SNPs). These were directly searched by DHPLC in a panel of SLE and MS patients and selected from databases and the literature. The SNP allele frequencies were determined on patient and control DNA pools by primer-extension genotyping and HPLC analysis. Moreover a panel of HLA typed SLE and control individuals were individually genotyped for the PRL G-1149T polymorphism previously described to be associated with SLE. No statistically significant difference in the allele distribution was observed for any of the tested variations.
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PMID:Prolactin and prolactin receptor gene polymorphisms in multiple sclerosis and systemic lupus erythematosus. 1255 30

The aim of the study was to evaluate the association between hyperprolactinemia and T lymphocyte activation through the soluble IL-2 receptor (sIL-2R) in systemic lupus erythematosus (SLE) patients. Seventy SLE patients, 18 of them with hyperprolactinemia (HPRL), were compared with 18 normoprolactinemic (NPRL) patients and 10 age-matched healthy blood-bank donor women. Patients were evaluated by means of the SLE activity index (SLEDAI). Total serum IgG and sIL-2R levels were determined by an ELISA assay. Differences between sIL-2R and IgG serum levels in patients and controls were examined by Kruskal-Wallis analysis and a Spearman r correlation to determine the association between sIL-2R, IgG and prolactin (PRL) levels. IgG and sIL-2R serum levels did not differ significantly between HPRL and NPRL patients: 1827.3 (1428-2226) vs 2028.8 (1586-2467) mg/dl and 882.2 (511-1254) vs 740.1 (534-946.4) U/ml, respectively (confidence interval 95%). In the total SLE group, sIL-2R and IgG serum levels were positively associated (P = 0.0009), however, this was not the case for sIL-2R and PRL (P > 0.49). We did not demonstrate an association between HPRL and lymphocyte activation measured through serum sIL-2R in female patients with SLE.
Lupus 2003
PMID:Lack of association between hyperprolactinemia and soluble IL-2 receptor levels in systemic lupus erythematosus. 1263 Jul 54

Prolactin is not only a lactigenic hormone but also an immunomodulator involved in lymphocyte survival, activation and proliferation. There is increasing data implicating prolactin in autoimmunity, and specifically in SLE. Increased serum prolactin levels have been reported in lupus patients of both genders, and have been associated with accelerated disease expression and early mortality in lupus-prone mice. Furthermore, suppression of prolactin secretion with bromocriptine provides beneficial effects in murine lupus, and perhaps in some SLE patients as well. Treatment with prolactin that causes mild to moderate hyperprolactinemia, similar to that present in SLE patients, breaks tolerance and induces a lupus-like illness in non-spontaneously autoimmune mice with a susceptible genetic background. These immuno stimulatory effects of prolactin are mediated by a decrease in negative selection and the maturation of autoreactive B cells to the follicular subset. Consistent with the fact that follicular B cells are T cell dependent, CD4+ T cells are necessary for the prolactin-mediated break down of B cell tolerance. In mice, the effects of prolactin on the immune system are genetically determined, suggesting that only a subset of SLE patients are likely to have a prolactin-responsive disease. The manipulation of serum prolactin or, even more specifically, follicular B cells that are susceptible to the immuno stimulatory effects of prolactin, may provide novel therapeutic options for those SLE patients with a prolactin-modulated disease.
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PMID:Prolactin as a modulator of B cell function: implications for SLE. 1519 67

Hyperprolactinemia without clinical manifestations has been reported in some patients with systemic lupus erythematosus (SLE) because an increase of prolactin (PRL) is produced due to the BIG/BIG molecular variant (molecular variant < 150 kD). This research project aimed to determine levels of PRL: its bioactive form, the little nonglycosylated form (NGPRL) and variants with decreased bioactivity such as the BIG/BIG and the little glycosylated (GPRL), in 29 women and five men with SLE. PRL was assayed by IRMA with a kit from Immunotech Laboratory, the BIG/BIG form by precipitation with polyethyleneglycol 6000, and the NGPRL and GPRL by chromatography on Concanavalin-A- Sepharose. Increased PRL was detected in seven patients (20.6%) of whom three had increased BIG/BIG, six had increased GPRL and only four had increased NGPRL. The three cases with increased BIG/BIG were contrasted by chromatography on Sephadex G-100. No increased PRL or any of the other variants assayed were found in men. Results were similar when PRL was evaluated in the same blood samples by a different IRMA (DPC Laboratory). The etiology of the hyperprolactinemia in some of these patients is unknown, but their lack of symptoms (galactorrhea or amenorrhea) could be due to the BIG/BIG forms and basically to the glycosylation of the hormone. As for the relation between PRL and SLE activity, we found that hyperprolactinemic patients were younger, had a shorter history of illness, although it was not statistically significant, and a higher SLEDAI score. This would indicate a relation between hyperprolactinemia and lupus activity. The patients with increased BIG/BIG form also had a very active illness at the time of the study.
Lupus 2004
PMID:Analysis of molecular heterogeneity of prolactin in human systemic lupus erythematosus. 1546 86

Autoimmune factors are involved in some of the cases of reproductive failure. These factors entail several autoantibodies, especially in patients having systemic lupus erythematosus (SLE) or the antiphospholipid syndrome (APS). These autoantibodies include mainly antibodies directed to phospholipid such as cardiolipin, phosphatidylserine, phosphatidylethanolamine or phospholipids binding glycoproteins such as beta2glycoprotein-I, annexin V, prothrombin and protein-Z. There are also some other autoantibodies directed to laminin-I, thromboplastin, mitochondrial antibodies of the M5 type, corpus luteum, prolactin, poly (ADP-ribose), thyroglobulin and more, which were also found in SLE or APS patients with reproductive failure. Moreover, the presence of additional autoantibodies directed to actin, enolase, cubilin and others, needs further investigation to support a firm association to reproductive failure in women. Future studies are likely to help to determine and expand the number of autoantibodies screened in these patients, as well as by the use of proteomics technology, to determine peptides resembling the epitope specificities associated with the specific clinical manifestations.
Lupus 2004
PMID:Autoantibodies associated with reproductive failure. 1548 94

Some cases of reproductive failure with autoimmune background are characterized by the involvement of autoantibodies. This occurs mainly in patients having systemic lupus erythematosus or antiphospholipid syndrome. The autoantibodies associated with reproductive failure include: a) antibodies which directly bind phospholipid (e.g., cardiolipin, phosphatidylserine, phosphatidylethanolamine); b) antiphospholipid Abs which bind the phospholipid via phospholipid-binding glycoproteins such as beta2glycoprotein-I, annexin V and prothrombin; c) autoantibodies directed to laminin-I, actin, thromboplastin, the corpus luteum, prolactin, poly (ADP-ribose), thyroglobulin and mitochondrial antibodies of the M5 type. This paper will focus on the association of antiphosphatidylserine autoantibodies and reproductive failure. Future studies are likely to help to identify peptides resembling the epitope specificities associated with the specific clinical manifestations.
Lupus 2004
PMID:Antiphosphatidylserine antibodies and reproductive failure. 1548 98

There is much interest in the possibility that prolactin influences disease activity in systemic lupus erythematosus (SLE). We present the first reported pediatric case of prolactinoma associated with SLE, in a 13-year-old white female. The diagnosis of SLE was based on the presence of arthritis, antinuclear antibodies, and double-stranded DNA, and a chest radiograph showing pleural fluid. The diagnosis of pituitary prolactinoma was based on the histologic features and the presence of amenorrhea, galactorrhea, and an elevated serum prolactin level. Neurosurgical resection and medical therapy with bromocriptine mesylate were independently associated with decreased prolactin levels, loss of arthritis, and reduced levels of inflammatory mediators.
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PMID:First reported pediatric case of systemic lupus erythematosus associated with prolactinoma. 1552 90

Much progress has been made in the understanding of the impact of the neuroendocrine immune interactions and the pathogenic role in systemic lupus erythematosus, clinically and at the molecular level. This article focuses on the intertwining networks that involve the hypothalamic-pituitary-adrenal axis, cytokines within the central nervous system, and the sympathetic system. Hormones (estrogen, prolactin, gonadotropin-releasing hormone, and leptin) play an important role as immunomodulatory agents.
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PMID:The neuroendocrine-immune interactions in systemic lupus erythematosus: a basis for understanding disease pathogenesis and complexity. 1563 61


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